Parkinson’s disease (PD) is a neurodegenerative illness and has a common onset between the ages of 55 and 65 years. There is progressive development of both motor and non-motor symptoms, greatly affecting one’s overall quality of life. While there is no cure, various treatments have been developed to help manage the symptoms of PD. Management of PD is a growing field and targets new treatment methods, as well as improvements to old ones. Pharmacological, surgical, and therapeutic treatments have allowed physicians to treat not only the main motor symptoms of PD, but target patient-specific problems as they arise. This review discusses both the established and new possibilities for PD treatment that can provide patient-specific care and mitigate side effects for common treatments.
Worldwide, spinal cord injury (SCI) affects around 500,000 people each year and results in significant morbidity. The primary insult to the spinal cord occurs at the time of the initial injury, which may result from a contusion, laceration or more rarely a transection. Secondary damage in SCI is more insidious and subacute; it is the result of a combination of an inflammatory response, vascular changes and ionic dysregulation. Early clinical intervention is vital after the acute, primary insult to ensure the best possible outcomes for these patients. Current evidence on the demographics and mechanisms, underlying basic science and management strategies of spinal cord injuries are outlined.
Multiple sclerosis (MS) is a lifelong inflammatory demyelinating disease of the central nervous system (CNS). While there has been substantial progress in the development of therapeutic strategies for relapsing disease, the field has lagged behind in its understanding and management of progressive stages of the disease, including secondary progressive and primary progressive MS, respectively. It is now thought that distinct but temporally overlapping mechanisms underlie relapsing and progressive aspects of the disease. Relapsing disease is characterized by waves of peripheral immune cell activation and CNS infiltration leading to focal destruction of the white matter, while progressive disease is thought to be driven by chronic, low-grade multifocal inflammation contained within the CNS compartment. Specifically, peripheral B cells, T cells, and myeloid cells take up residence within niches of the inflamed CNS, such as the leptomeninges and the Virchow-Robin spaces, where complex interactions between peripheral and CNS resident cells serve to maintain these cellular aggregates and further propagate CNS injury. In particular, immune infiltrates within the meninges are tightly associated with a specific form of cortical injury, termed subpial cortical demyelination, which is thought to be a key pathologic driver of disease progression. Cortical injury in the MS brain likely occurs via a combination of multiple immune-mediated and degenerative processes, perhaps including the production of diffusible toxic mediators by peripheral immune cells retained within the meninges. A better understanding of the interplay between peripheral immune and CNS resident cells is not only relevant to our concept of the disease process, but also represents a novel target for therapeutic intervention that is more specific to progressive disease biology. This review will focus on the role of CNS-compartmentalized inflammation in the development of cortical injury in MS, with a particular emphasis on the importance of immune-CNS crosstalk in disease progression.
Neuroimmunology and Neuroinflammation is an open access journal, with focuses on neuroimmunology and neuroinflammation research, and coverage extending to other basic and clinical studies related to neuroscience.
Neuroaxonal loss is believed to underpin the progressive disability that characterizes multiple sclerosis (MS). While focal inflammatory demyelination is a principal cause of acute axonal transection and subsequent axonal degeneration, the gradual attrition of permanently demyelinated axons may also contribute to tissue damage, particularly in the progressive phase of the disease. Therefore, remyelination is considered a putative neuroprotective strategy. In this article, we review the potential pitfalls of remyelination trials, provide a framework for their appropriate design and temper the expectations, at times unrealistic, of researchers, regulators and the pharmaceutical industry.
